Expression of androgen receptor coactivator ARA70/ELE1 in androgenic alopecia

J Cutan Pathol. 2005 Sep;32(8):567-71. doi: 10.1111/j.0303-6987.2005.00397.x.


Background: Androgens have been implicated in androgenic alopecia as evidenced by the increased cutaneous expression of androgen receptor (AR), 5alpha-reductase, and decreased aromatase. Abnormalities of the AR-signal transduction pathway probably participate in the development of androgenic alopecia. ARA70/ELE1 is an AR coactivator with two isoforms, one full-length form (ARA70alpha/ELE1alpha), and an internally deleted form (ARA70beta/ELE1beta). We decided to examine the cutaneous expression of both isoforms in male androgenic alopecia.

Methods: Formalin-fixed, paraffin-embedded tissue sections from seven subjects with androgenic alopecia with matched punch biopsies from non-balding and balding areas were examined by in situ hybridization.

Results: Expression of at least one of the two probes for ARA70/ELE1 was present in all phases of the hair-growth cycle in all epithelial hair structures except for the inner root sheath. The dermal papilla and hair bulb expressed only the short (beta) but not the long (alpha) form of ARA70/ELE1. In situ labeling for ARA70beta/ELE1beta was weaker in the dermal papilla of balding recipient areas than those from donor ones.

Conclusions: Our data further support that the hair growth is regulated by androgens. The differential expression pattern of ARA70/ELE1 suggests that this key androgen receptor coactivator is involved in androgenic alopecia. Lee P, Zhu C-C, Sadick NS, Diwan AH, Zhang PS, Liu JS, Prieto VG. Expression of androgen receptor coactivator ARA70/ELE1 in androgenic alopecia.

MeSH terms

  • Alopecia / metabolism*
  • Alopecia / pathology
  • Biomarkers / metabolism
  • Biopsy
  • Hair Follicle / growth & development
  • Hair Follicle / metabolism*
  • Hair Follicle / pathology
  • Humans
  • In Situ Hybridization
  • Male
  • Nuclear Receptor Coactivators
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism*
  • Protein Isoforms
  • RNA, Messenger / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*


  • Biomarkers
  • NCOA4 protein, human
  • Nuclear Receptor Coactivators
  • Oncogene Proteins
  • Protein Isoforms
  • RNA, Messenger
  • Transcription Factors